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830 > IHD Patho > Flashcards

IHD Patho Flashcards

1
Q

Myocardial Ischemia

A

Lack of oxygen and reduced blood flow to the myocardium resulting in an imbalance between myocardial oxygen supply and demand

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2
Q

Myocardial Infarction

A

Necrosis (death) of heart muscle caused by an imbalance between oxygen supply and demand

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3
Q

Angina Pectoris

A

“Chest pain”; pain or discomfort in the chest or adjacent areas which is due to myocardial ischemia

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4
Q

Silent Ischemia

A

Painless episodes of myocardial ischemia (75% of all ischemia)

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5
Q

Silent Infarction

A

Infarction occurring without chest pain or other common symptoms of ischemia; about 20% of all first infarcts

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6
Q

Acute Coronary Syndrome

A

Unstable angina or acute myocardial infarction

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7
Q

Myocardial Oxygen Demand

A
  1. Heart Rate
  2. Wall Tension
  3. Contactility
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8
Q

Wall Tension

A
  • Related to ventricular volume and wall pressure

- Preload v.s. Afterload

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9
Q

Myocardial Oxygen Supply

A
  1. Coronary Blood Flow
  2. Collaterals
  3. Autoregulation
  4. Other factors that regulate coronary blood flow
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10
Q

Coronary Blood Flor

A
  • Increased oxygen demand must be met by an increase in coronary blood flow
  • Coronary blood flow can normally increase 5x resting value
  • Coronary blood flow occurs primarily during diastole
  • May be altered by fixed obstruction or vasospasm
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11
Q

Collaterals

A
  • Provide blood flow when major vessels are obstructed
  • Development enhanced by gradual coronary occlusion, exercise, severe anemia
  • May prevent a myocardial infarction in the presence of total occlusion
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12
Q

Autoregulation

A

-As larger coronary arteries become occluded or stenotic, smaller vessels dilate to maintain coronary blood flow

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13
Q

Other Factors

A
  • Neural (symp v.s. parasymp.)
  • Endothelium - EDRF, endothelin, prostaglandins, others
  • Metabolic - oxygen, carbon dioxide, adenosine
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14
Q

Oxygen Extraction

A
  • At rest, 65-75% of oxygen passing through myocardium is extracted
  • With increased oxygen demand, oxygen extraction can approach 80%
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15
Q

Blood Oxygen Content

A
  • Hemoglobin/hematocrit

- Arterial blood gases

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16
Q

Types of Ischemic Heart Disease

A
  1. Chronic Stable Angina
  2. Unstable Angina
  3. Vasospastic Angina (Prinzmetal’s Variant)
  4. Myocardial Infarction (MI)
17
Q

Chronic Stable Angina

A
  • Associated with a certain level of physical activity or emotional stress
  • Relieved by rest or nitroglycerin
18
Q

Unstable Angina

A
  • Angina of new onset, usually within one month and brought on by minial exertion
  • Development of crescendo (more severe) pain superimposed on preexisting exertion-related angina
  • Any change in angina frequency, intensity, or duration
  • Pain at rest
  • No elevated cardiac enzymes or ST-segment elevation
19
Q

Vasospastic Angina

A
  • Occurs in patients with or without coronary heart disease and is due to a spasm of a coronary artery that decreases myocardial blood flow
  • More likely to experience pain at rest and in the early morning hours
  • Pain not usually brought on by exertion or emotional stress or relieved by rest
  • Occurs more often in smokers, young patients, with illicit drug use, and with alcohol withdrawal
20
Q

Myocardial Infarction

A
  • Most common due to artherosclerotic thrombosis
  • Coronary spasm and coronary embolus may also cause infarction
  • ST-segment and Non-ST segment elevation MI
21
Q

STEMI

A
  • ST-segment elevation MI
  • MI characterized by ST-segment elevation on the ECG in at least 2 contiguous leads of >= 2 mm in men or >= 1.5 mm in women in leads V2-V3 and/or ?= 1 mm in other contiguous chest leads or the limb leads
  • More extensive infarct
  • Higher hospital mortality rate
  • Elevated cardiac enzymes
22
Q

NSTEMI

A
  • Non-ST-segment elevation MI
  • Damage to myocardium is not as extensive
  • Increased likelihood of developing post-infarction angina and early reinfarction
  • Elevated cardiac enzymes
23
Q

Type I MI

A
  • Spontaneous MI
  • Due to atherosclerotic plaque rupture and thrombus formation
  • Vast majority of MI
24
Q

Type II MI

A
  • Due to ischemic imbalance
  • NOT due to plaque rupture, but end result is in inadequate oxygenation of myocardial tissue
  • EX: coronary vasospasm, hypotension, anemia, etc.
25
Q

Type 3 MI

A
  • Fatal MI in the setting of no cardiac biomarkers
  • REsults in death and suspected based on symptoms and ECG findings
  • No cardiac biomarkers obtained
26
Q

Type 4a MI

A
  • Due to PCI
  • Confirmed by troponin elevations and one or more of the following:
    1. Symptoms of ischemia
    2. ECG changes
    3. Angiographic evidence of coronary artery obstruction
    4. Imaging evidence of myocardial damage
27
Q

Type 4b MI

A
  • Due to stent thrombosis

- Confirmed by an increase in cardiac biomarkers

28
Q

Type 5 MI

A
  • Due to CABG
  • Confirmed by the increase in cardiac biomarkers and one or more of the following:
    1. New Q waves or left bundle branch block on ECG
    2. Angiographic evidence of new coronary artery obstruction
    3. Imaging evidence of myocardial damage
29
Q

Patho of Atherosclerosis

A
  1. Phase 1: small plaque that is present in most people < 30 y.o., usually progresses slowly
  2. Phase 2: Plaque, not necessarily stenotic, with high lipid content and is prone to rupture
  3. Phase 3: Plaque rupture with mural thombosis formation, leads to an increase in artery stenosis and possibly angina
  4. Phase 4: Plaque rupture leading to an acute coronary occlusion, leads to unstable angina, AMI, or ischemic sudden death
  5. Phase 5: Severely stenotic or occlusion plaques organized by connective tissue, may become complicated by a thrombus and/or myoproliferative response leading to an acute silent occlusive process
30
Q

Plaque Rupture

A
  • Most complications of atherosclerosis are due to plaque rupture
  • Rupture tends to occur at junctions, branches, or bends in the vessel
31
Q

Clot Formation

A
  • Platelet deposition: first step in hemostasis and thrombus formation, increases with an increase in shear force
  • Platelet activation causes conformational change in GP IIb/IIIa receptor, allowing it to bind to fibrinogen
  • Fibrinogen cross-links develop and form bridges to otehr platelets, facilitating aggregation and ultimately platelet plug
  • Platelets generate thrombin and convert fibrinogen to fibrin which converts white thrombus to a stable red-thrombus
  • Plaque composition may be MOST important determinant for plaque rupture/fissure
32
Q

Glycoproteins

A
  • Different GP adhere to various adhesive proteins found in subendothelial matrix which are exposed by vessel damage
  • GP Ib: binds von Willebrand factor
  • GP Ia/IIA: binds collagen
  • GP Ic/IIa: binds fibronectin
  • GP IIb/IIa: plays a secondary role in platelet adhesion
33
Q

History/Risk Factor Assessment

A
  • Part of Diagnosis of IHD
  • No physical findings are specific for angina
  • Characteristics of pain
  • Laboratory assessment is not helpful except for cardiac enzymes
  • Patient’s cardiac risk factors
  • Pain with unstable angina typically lasts 10-20 minutes
  • Pain with non-ST-elevation MI typically lasts up to an hour
  • Pain with an ST-elevation MI typically lasts > 1 hour
34
Q

ECG

A
  • Used in diagnosis of IHD
  • Resting ECG is normal in about 30-50% of patients with angina
  • ST-T wave changes
  • Q waves with infarction
  • Use of ambulatory monitoring to detect silent ischemia
35
Q

Exercise Tolerance Testing (ETT)

A
  • Used in diagnosis of IHD
  • Useful for assessing the severity and prognosis of CAD
  • Positive test indicated by angina, ECG changes, or dysrhythmias
  • Abnormal BP or HR response may signal CAD
36
Q

Radionuclide Imaging

A
  • Used in diagnosis of IHD
  • Patient is stressed with either exercise or pharmacologically and then myocardial imaging performed using either sestamibi or thallium
  • Defect in myocardial uptake of sestamibi or thallium indicates ischemia or infarction
  • More expensive than ETT
37
Q

Radionuclide Imaging Useful for patients….

A
  • Unable to exercise completely
  • Asymptomatic with abnormal results on ETT
  • Men with typical angina who have “negative” results on ETT
  • Women with typical angina who have equivocal ETT results
  • Patients with known CAD to determine myocardial viability
38
Q

Coronary Angiography

A
  • Used in diagnosis of IHD and definitive diagnosis of CAD
  • Allows determination of location and extent of atherosclerosis
  • Used when bypass surgery or angioplasty are being contemplated for therapy
  • Does not give functional information
39
Q

Cardiac Enzymes

A
  • Used in diagnosis of IHD
  • Creatine kinase (CK or CPK)
  • Isoenzymes: MM (muscle), BB (brain), MB (myocardium)
  • Troponins I and T

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